Modulation of rat oligodendrocyte precursor cells by the chemokine CXCL12
Modulation of rat oligodendrocyte precursor cells by the chemokine CXCL12
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DOI：
10.1097/01.wnr.0000227985.92551.9a
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发表时间：
2006-07-31
期刊：
影响因子：
1.7
通讯作者：
Stangel, Martin
中科院分区：
文献类型：
--
作者：
Maysami, Samaneh;Nguyen, Dan;Stangel, Martin
少突胶质细胞前体细胞的迁移、增殖和分化对于中枢神经系统中髓磷脂的组装至关重要。因此，有关这些前体细胞调节的知识对于了解脱髓鞘疾病中的发育髓鞘形成和髓鞘再生非常重要。在这里，我们证明原代大鼠少突胶质细胞前体细胞表达趋化因子受体 CXCR4。用配体 CXCL12 (SDF-I α) 刺激会导致细胞内 Ca2+ 升高。此外，10 ng/ml CXCL12 增强了前体细胞向成熟少突胶质细胞的分化。 CXCL12 抑制向生长因子条件培养基的迁移，而增殖仅受到轻微调节。使用 G 蛋白拮抗剂阻断 CXCL12 对迁移和分化的影响。这些数据表明 CXCL12 和少突胶质细胞 CXCR4 受体在中枢神经系统脱髓鞘疾病的发育髓鞘形成和修复过程中发挥作用。
Migration, proliferation, and differentiation of oligodendrocyte precursor cells are essential for the assembly of myelin in the central nervous system. Knowledge on the regulation of these precursor cells is therefore of great importance for the understanding of developmental myelination and remyelination in demyelinating diseases. Here, we show that primary rat oligodendrocyte precursor cells express the chemokine receptor CXCR4. Stimulation with the ligand CXCL12 (SDF-I alpha) leads to intracellular Ca2+ elevation. Furthermore, 10 ng/ml CXCL12 augmented differentiation of precursors into mature oligodendrocytes. Migration toward growth factor conditioned medium was inhibited by CXCL12, while proliferation was only slightly modulated. The effect of CXCL12 on both migration and differentiation was blocked using a G protein antagonist. These data suggest a role for CXCL12 and oligodendroglial CXCR4 receptors during developmental myelination and repair in demyelinating diseases of the central nervous system.